血栓素B2对急性主动脉夹层诊治的指导价值

目的 探讨血栓素B2(thromboxane B2,TxB2)对主动脉夹层诊治的指导价值.方法 选取广东省人民医院2016至2017年采集的受试者血浆样本72例:急性主动脉夹层(acute aortic dissection,AAD)患者24例,其中A型主动脉夹层(AAD-A)12例,B型主动脉夹层(AAD-B)12例...     

心功能不全(Ⅲ级)患者采用团注追踪技术行冠状动脉血管造影的可行性

目的 探讨心功能不全(Ⅲ级)患者行冠状动脉血管造影的可行性.方法 选取聊城市人民医院2017年1月至2019年12月收治的心功能不全(Ⅲ级)患者40例,根据扫描技术不同将患者随机分为A组与B组,每组各20例.A组应用小剂量预测峰值(test bolus)技术小剂量测试(20ml对比剂),监测峰值时间(T1);B组应用团...     

经皮封堵术在55岁以上高危卵圆孔未闭患者中的临床疗效分析

目的 探讨年龄大于55岁的高危卵圆孔未闭(patent foramen ovale,PFO)患者行经皮封堵术的必要性、临床疗效及预后.方法 选取2015年1月至2018年12月衡水市人民医院心外科行PFO封堵术的患者共60例,其中年龄大于55岁的患者24例(A组),年龄小于55岁患者36例(B组);观察A、B两组患者的...     

艾滋病合并人微小病毒B19感染导致纯红细胞再生障碍性贫血5例临床特征分析

目的 分析艾滋病合并人微小病毒B19(HPV B19)感染导致纯红细胞再生障碍性贫血临床特点.方法 回顾性分析2018年6月至2019年12月在广州市第八人民医院住院部收治的5例艾滋病合并HPV B19感染导致纯红细胞再生障碍性贫血患者的临床资料.结果 5例艾滋病患者中,男性4例,年龄14～43岁;2例接受ART时间＜...     

人类免疫缺陷病毒感染、结核分枝杆菌感染和共感染患者的CD8+T细胞耗竭状态

目的分析人类免疫缺陷病毒(human immunodeficiency virus, HIV)感染、结核分枝杆菌(Mycobacterium tuberculosis, MTB)感染, 以及共感染患者的CD8+T细胞耗竭状态。方法纳入2019年8月至2020年1月无锡市第五人民医院和太仓市第一人民医院所收治的HIV感染和(或)MTB感染患者87例, 其中HIV感染18例, 活动性结核(active tuberculosis, ATB)34例, 潜伏性结核(latent tuberculosis, LTB)19例, HIV感染合并ATB 7例, HIV感染合并LTB 9例, 同时纳入11名健康对照者。收集所有受试者的外周血, 进行全血细胞表面染色和细胞内染色, 使用流式细胞术检测CD8+T细胞上的活化分子CD62配体、CD44、CD127, 转录因子脱中胚蛋白(eomesodermin, EOMES)、T细胞因子1(T cell factor 1, TCF-1)、T盒转录因子(T-box expressed in T cells, T-bet)、B淋巴细胞诱导成熟蛋白1(B lympho...     

高三酰甘油血症腰围表型与SYNTAX评分和血液流变学及内皮功能的相关性

目的 分析高TG血症-腰围表型(HTWC)与SYNTAX评分、血液流变学、内皮功能的关系及对心血管事件的预测价值.方法 选择2017年12月～2019年11月济南市人民医院心内科收治的冠心病患者230例,根据TG水平和腹型肥胖分为TG和腰围正常组79例(A组)、单纯高TG组66例(B组)、单纯腹型肥胖组50例(C组)、...     

稽留流产患者8-异构前列腺素、超氧化物歧化酶、腺苷脱氨酶、转录因子κB和诱导型一氧化氮合酶表达情况及其临床意义

目的分析稽留流产患者8-异构前列腺素(8-isoprostane)、超氧化物歧化酶(SOD)、腺苷脱氨酶(AOA)、转录因子κB(NF-κB)、诱导型一氧化氮合酶(iNOS)表达情况及其临床意义。方法选取佛山市南海区第二人民医院2014年5月—2017年5月收治的稽留流产患者50例作为研究组,另选取同期正常妊娠者50例作为对照组。比较两组受试者血清及绒毛蜕膜组织中8-isoprostane、SOD、AOA、NF-κB、iNOS水平。结果研究组患者血清及绒毛蜕膜组织中8-isoprostane、NF-κB、iNOS水平高于对照组,SOD水平低于对照组(P<0.05);两组受试者血清和绒毛蜕膜组织中AOA水平比较,差异无统计学意义(P>0.05)。结论稽留流产患者血清和绒毛蜕膜组织中8-isoprostane、NF-κB、iNOS水平升高,SOD水平降低,其可作为稽留流产的预测因子。     

隐源性机化性肺炎患者血清半乳凝素9水平变化及其临床意义研究

目的分析隐源性机化性肺炎(COP)患者血清半乳凝素9(Galectin-9)水平变化及其临床意义。方法选取2009年5月—2015年12月在连云港市第一人民医院呼吸内科住院治疗的社区获得性肺炎(CAP)患者26例(A组)和COP患者26例(B组),另选取同期连云港市第一人民医院体检健康者26例作为对照组。比较3组受试者血清Galectin-9水平,血清Galectin-9水平与COP患者COP面积比的相关性分析采用Pearson相关性分析,比较COP患者治疗前和治疗两周后血清Galectin-9水平和COP面积比。结果 A组和B组患者血清Galectin-9水平高于对照组,B组患者血清Galectin-9水平高于A组(P0.05)。Pearson相关性分析结果显示,血清Galectin-9水平与COP患者COP面积比呈正相关(r=0.784,P0.05)。COP患者治疗两周后血清Galectin-9水平和COP面积比均低于治疗前(P0.05)。结论 COP患者血清Galectin-9水平明显升高,且血清Galectin-9水平可用于辅助诊断COP、评估患者病情严重程度及预后。     

盐酸氨溴索对慢性阻塞性肺疾病诱导痰巨噬细胞NF-κB的影响

目的探讨盐酸氨溴索对稳定期慢性阻塞性肺疾病(COPD)患者诱导痰巨噬细胞核转录因子kappaB(NF-κB)的影响。方法将2004年1~10月河南省人民医院门诊及住院47例稳定期COPD患者,随机分为治疗组和对照组,治疗组除给予常规治疗外,加用盐酸氨溴索(每次30 mg,每日3次,连用2个月);对照组仅给予常规治疗。观察治疗前后所有患者超氧化物歧化酶(SOD)活力和丙二醛(MDA)浓度,诱导痰上清液IL-8质量浓度及巨噬细胞NF-κB P65表达。结果两组治疗后IL-8、NF-κB水平较治疗前均下降,差异有显著性意义(P<0.05),治疗组治疗后的IL-8、NF-κB下降较对照组显著(P<0.05)。结论盐酸氨溴索可降低稳定期COPD患者诱导痰巨噬细胞NF-κB表达程度。     

血清白介素17及干扰素γ水平与急性冠脉综合征患者心功能的相关性研究

目的探讨血清白介素17及干扰素γ水平与急性冠脉综合征(ACS)患者心功能的相关性。方法选取2014年1月—2017年1月常州市第四人民医院心内科收治的ACS患者62例,根据疾病类型分为A组[急性心肌梗死(AMI)]与B组[不稳定型心绞痛(UAP)],每组31例;另选取同期于常州市第四人民医院体检健康者31例作为对照组。比较3组受试者血清白介素17和干扰素γ水平及心功能指标;血清白介素17、干扰素γ水平与ACS、AMI患者心功能指标的相关性分析采用Pearson相关性分析。结果 A、B组患者血清白介素17、干扰素γ水平高于对照组(P0.05);A组患者血清干扰素γ水平高于B组(P0.05)。A组患者左心室射血分数(LVEF)、左心室短轴缩短率(LVFS)低于对照组、B组,左心室舒张末期内径(LVEDD)长于对照组、B组(P0.05)。Pearson相关性分析结果显示,血清白介素17水平与ACS患者LVEF呈负相关(r=-0.301,P0.05);血清白介素17水平与AMI患者LVEF呈负相关(r=-0.523,P0.05),血清干扰素γ水平与AMI患者LVEF、LVEDD呈负相关(r值分别为-0.125、-0.011,P0.05)。结论血清白介素17及干扰素γ水平与ACS患者心功能密切相关,可在一定程度上反映ACS患者病情严重程度。     

Expression of B7-H4 and hepatitis B virus X in hepatitis B virus-related hepatocellular carcinoma

AIM: To investigate the expression and clinical significance of B7-H4 and hepatitis B virus X(HBx) protein in hepatitis B virus-related hepatocellular carcinoma(HBV-HCC).METHODS: The expression of B7-H4 in the human HCC cell lines Hep G2 and Hep G2.2.15 were detected by western blot, flow cytometry, and immunofluorescence. The expression of B7-H4 and HBx in 83 HBV-HCC was detected by immunohistochemistry, and the relationship with clinicopathological features was analyzed. Paraffin sections were generated from 83 HBV-HCC patients(22 females and 61 males) enrolled in this study. The age of these patients ranged from 35 to 77 years, with an average of 52.5 ± 11.3 years. All experiments were approved by the Ethics Committees of the Second Affiliated Hospital, Zhejiang University School of Medicine.RESULTS: B7-H4 was significantly upregulated in Hep G2.2.15 cells compared to Hep G2 cells. Specifically, the protein expression of B7-H4 in the lysates of Hep G2 cells was more than that in Hep G2.2.15 cells. In addition, HBx was expressed only in Hep G2.2.15 cells. Similar data were obtained by flow cytometry. The positive rates of B7-H4 and HBx in the tissues of 83 HBV-HCC patients were 68.67%(57/83) and 59.04%(49/83), respectively. The expression of HBx was correlated with tumor node metastases(TNM) stage, and the expression of B7-H4 was positively correlated with HBx(rs = 0.388; p 0.01). The expression level of B7-H4 in HBx-positive HBV-HCC tissues was substantially higher than that in HBx-negative HBV-HCC tissues. The expression level of B7H4 was negatively related to tumor TNM stage.CONCLUSION: Higher expression of HBx and B7-H4 was correlated with tumor progression of HBV-HCC, suggesting that B7-H4 may be involved in facilitating HBV-related hepatocarcinogenesis.     

慢性乙型肝炎患者肝细胞内乙型肝炎核心抗原阳性的临床意义

目的探讨CHB患者肝组织HBcAg阳性的意义。方法对200例CHB患者应用荧光聚合酶链反应（FQ-PCR）法精确定量检测血清HBV DNA含量。患者均检测血清中HBeAg含量,同时进行肝活组织检查,应用免疫组织化学技术检测HBcAg情况,并进行相关性分析。结果按测定血清HBV DNA水平,分为A组（＜3 log10拷贝/ml）20例,B组（≥3 log10拷贝/ml-＜5 log10拷贝/ml）13例,C组（≥5 log10拷贝/ml～＜6 log10拷贝/ml）24例,D组（≥6 log10拷贝/ml～＜8 log10拷贝/ml）116例,E组（≥8 log10拷贝/ml）27例。肝组织HBcAg阳性者175例,占87．5％,A组HBcAg阳性率55．0％（11/20）,B组53．8％（7/13）,C组75．0％（18/24）,D组96．6％（112/116）,E组100．0％（27/27）,HBcAg阳性率与血清HBV DNA水平之间呈显著正相关（r=0．80,P＜0．01）。血清HBV DNA水平高低与HBeAg阳性率之间呈显著正相关（r=0．47,P＜0．01）。其中20例HBV DNA阴性者中（A组）,HBeAg阳性者5例（25％）,HBcAg阳性者11例（55％）；15例HBV DNA阴性且HBeAg阴性者中有7例HBcAg阳性,占46．7％。结论CHB患者肝组织HBcAg阳性能更可靠地反映肝细胞内HBV复制状态。检测肝组织内HBcAg对CHB患者疗效评价和对治疗反应性的预测更具有临床意义。     

Advances in treatment and prevention of hepatitis B

Chronic hepatitis B(CHB) continues to contribute to worldwide morbidity and mortality significantly. Scientists, clinicians, pharmaceutical companies, and health organizations have dedicated substantial Intellectual and monetary resources to finding a cure, increasing immunization rates, and reducing the global burden of CHB. National and international health-related organizations including the center for disease control, the national institute of health, the American Association for the study of liver disease(AASLD), The European association for the study of the Liver(EASL), The Asia Pacific association for the study of the Liver(APASL) and the world health organization release periodic recommendations for disease prevention and treatment. Our review of the most recent guidelines by EASL, AASLD, APASL, and Taiwan Association for the Study of the Liver revealed that an overwhelming majority of cited studies were published before 2018. We reviewed Hepatitis B-related literature published 2018 onwards to identify recent developments and current barriers that will likely direct future efforts towards eradicating hepatitis B. The breakthrough in our understanding of the hepatitis B virus life cycle and resulting drug development is encouraging with significant room for further progress. Data from high-risk populations, most vulnerable to the devastating effects of hepatitis B infection and reactivation remain sparse. Utilization of systems approach, optimization of experimental models, identification and validation of next-generation biomarkers, and precise modulation of the human immune response will be critical for future innovation. Within the foreseeable future, new treatments will likely complement conventional therapies rather than replace them. Most Importantly, pragmatic management of CHB related population health challenges must be prioritized to produce real-world results.     

Treatment of chronic hepatitis B

SUMMARY. Chronic infection with the hepatitis B virus (HBV) is a major cause of worldwide morbidity and mortality. A large number of therapeutic approaches has been tried, including interferon (IFN), nucleoside analogues and immunomodulators. To date controlled clinical trials have shown that only IFN is of long-term value but many patients fail to respond to treatment. New approaches to treating patients with IFN-resistant hepatitis B are currently undergoing clinical and experimental evaluation, and it seems likely that new therapeutic agents will be available in the near future.     

Novel hepatitis B virus surface antigen mutations associated with occult genotype B hepatitis B virus infection affect HBsAg detection

The causative factors of occult hepatitis B infection are complicated and not yet been fully elucidated. Mutations in hepatitis B virus (HBV) S gene are one of the factors may contributing to occult infection. In this study, 89 blood donors with genotype B occult HBV infection were investigated. Fifty‐seven hepatitis B surface antigen (HBsAg)‐positive/HBV DNA‐positive blood donors served as control group for comparison. Occult HBV‐related mutations with a high incidence (P < .05) in the S gene were identified. To further verify these occult infection‐related mutations, a conservative full‐gene expression vector of HBV B genotype (pHBV1.3B) was constructed. Then, the mutant plasmids on the basis of pHBV1.3B were constructed and transfected into HepG2 cells. Extracellular as well as intracellular HBsAg was analysed by electrochemical luminescence and cellular immunohistochemistry. Ten occult infection‐related mutations (E2G, Q101R, K122R, M133T, D144E, G145R, V168A, S174N, L175S and I226S) were significantly more frequent in the occult infection group (P < .05). Five of the ten mutations (E2G, D144E, G145R, V168A and S174N) strongly decreased extracellular HBsAg level (P < .05) in the transfection system. Notably, the E2G mutation had the most significant impact on the ratio of extracellular HBsAg (3.8% vs pHBV1.3B) and intracellular HBsAg (239.3% vs pHBV1.3B) (P < .05), and the fluorescence density of E2G mutant HBsAg was significantly higher than that of pHBV1.3B (P < .0001). Hence, ten mutations were associated with genotype B occult HBV infection; E2G and V168A were novel mutations which we confirmed significantly affect HBsAg detection. E2G might cause HBsAg secretion impairment that results in intracellular accumulation and a decrease in HBsAg secretion.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.     

一种新的HBeAg阴性慢性乙型肝炎病毒变异机制

Objective To investigate mutation patterns in core promoter(CP)region of hepatitis B virus(HBV).Methods HBV DNA was extracted from sera of patients with chronic HBV infection.The CP sequence was amplified by polymerase chain reaction(PCR)and cloned into pMD19 T vector.The positive clones were then sequenced.The sequences were compared with known HBV genome in GenBank to identify the mutation sites and patterns of patients with chronic HBV infection.Results There were 74 clones from 21 patients with chronic HBV infection which were sequenced.The sequence comparisons showed that there was a 234-nucleotide deletion in CP region of HBV genome in 54 clones and a 245-nucleotide deletion in one clone.These deletion regions included CP,HBeAg initiation codon and direct repeat sequence(DR)Ⅰ regions,which named CP deletion(CPD).A1585T replacement mutation was also found in HBV strain with CPD,which indicated that there was linkage between these two mutations.Conclusions A novel mechanism of HBeAg negative chronic hepatitis B is observed,which includes deletions of CP and HBeAg initiation codon.Meanwhile,a simple and useful PCR method is developed to detect CPD.